Glucocorticoid receptor activation selectively hampers N-methyl-d-aspartate receptor dependent hippocampal synaptic plasticity in vitro

Wiegert, Olof; Pu, Zhenwei; Shor, S.; Joëls, Marian; Krugers, Harm J.

doi:10.1016/j.neuroscience.2005.05.039

Cited by 76 publications

(73 citation statements)

References 50 publications

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“…Specifically, it is thought that activation of hippocampal GRs by corticosterone leads to the blockade of glutamate uptake [20] which, consequently, leads to spillover of synaptically released glutamate by low-frequency stimulation, which then acts on extrasynaptic GluN2B-containing NMDARs, leading to the subsequent endocytosis of GluA2-containing AMPARs (Figure 1c). Such a proposed mechanism is in agreement with evidence that (i) GR activation selectively hampers NMDAR-dependent synaptic plasticity [37], and (ii) blocking glutamate uptake facilitates LTD by allowing glutamate release by low-frequency stimulation to activate extrasynaptic NMDARs [36]. GluN2B-containing NMDARs have also been implicated in mediating the impairing effects of stress during memory retrieval as assessed in rats during an object recognition memory task [38].…”

Section: Opinionsupporting

confidence: 84%

“…In the hippocampus, stress was systematically shown to impair long-term potentiation (LTP) while facilitating longterm depression (LTD) [94]. Glucocorticoid actions via GR and NMDARs have been implicated in these effects [37,69]. However, acute effects of glucocorticoids on LTP are not always detrimental.…”

Section: Opinionmentioning

confidence: 99%

“…More recently, epigenetic mechanisms -that are crucially involved in the regulation of gene transcription -have also been implicated in memory formation and maintenance [66]. Importantly, the activation of NMDARs, in addition to being required for many forms of synaptic plasticity and learning (Box 2) [67,68], has also been implicated in the effects of stress and glucocorticoids on hippocampal LTP and LTD [37,69] and in some forms of learning. For example, amygdaloid NMDARs (that play a crucial role in fear extinction [70]) have also been implicated in the facilitating effect of glucocorticoids on fear extinction [71,72].…”

Section: Trends In Neurosciencesmentioning

confidence: 99%

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Glucocorticoids act on glutamatergic pathways to affect memory processes

Sandi

2011

Trends in Neurosciences

148

117

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Section: Opinionsupporting

confidence: 84%

Section: Opinionmentioning

confidence: 99%

Section: Trends In Neurosciencesmentioning

confidence: 99%

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Glucocorticoids act on glutamatergic pathways to affect memory processes

Sandi

2011

Trends in Neurosciences

148

117

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“…This is in line with recent observations in the hippocampal CA1 area, showing that corticosterone can enhance long-term potentiation (LTP)-presently the best-described neurobiological substrate of learning and memory (Martin and Morris 2002;Morris 2003)-when the hormone is applied around the time of LTP induction , while it suppresses LTP when given several hours in advance (Alfarez et al 2002;Wiegert et al 2005).…”

supporting

confidence: 91%

“…An interval of 2 h was chosen to ensure that gene-mediated effects can take place Wiegert et al 2005;Morsink et al 2006). Contrary to what was seen with isoproterenol only or with concurrent perfusion of both hormones, isoproterenol did not affect synaptic responses after TBS if corticosterone was applied to the same slice a few hours earlier.…”

Section: Learning and Memory 361mentioning

confidence: 99%

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Pu¹,

Krugers²,

Joëls³

2007

Learn. Mem.

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Previous experiments in the hippocampal CA1 area have shown that corticosterone can facilitate long-term potentiation (LTP) in a rapid non-genomic fashion, while the same hormone suppresses LTP that is induced several hours after hormone application. Here, we elaborated on this finding by examining whether corticosterone exerts opposite effects on LTP depending on the timing of hormone application in the dentate gyrus as well. Moreover, we tested rapid and delayed actions by corticosterone on ␤-adrenergic-dependent changes in LTP. Unlike the CA1 region, our in vitro field potential recordings show that rapid effects of corticosterone do not influence LTP induced by mild tetanization in the hippocampal dentate gyrus, unless GABA A receptors are blocked. In contrast, the ␤-adrenergic agonist isoproterenol does initiate a slow-onset, limited amount of potentiation. When corticosterone was applied concurrently with isoproterenol, a further enhancement of synaptic strength was identified, especially during the early stage of potentiation. Yet, treatment with corticosterone several hours in advance of isoproterenol fully prevented any effect of isoproterenol on LTP. This emphasizes that corticosterone can regulate ␤-adrenergic modulation of synaptic plasticity in opposite directions, depending on the timing of hormone application.

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Dynamically changing effects of corticosteroids on human hippocampal and prefrontal processing

Henckens¹,

Pu²,

Hermans³

et al. 2011

Human Brain Mapping

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Stress has a powerful impact on memory. Corticosteroids, released in response to stress, are thought to mediate, at least in part, these effects by affecting neuronal plasticity in brain regions involved in memory formation, including the hippocampus and prefrontal cortex. Animal studies have delineated aspects of the underlying physiological mechanisms, revealing rapid, nongenomic effects facilitating synaptic plasticity, followed several hours later by a gene-mediated suppression of this plasticity. Here, we tested the hypothesis that corticosteroids would also rapidly upregulate and slowly downregulate brain regions critical for episodic memory formation in humans. To target rapid and slow effects of corticosteroids on neural processing associated with memory formation, we investigated 18 young, healthy men who received 20 mg hydrocortisone either 30 or 180 min before a memory encoding task in a double-blind, placebo-controlled, counter-balanced, crossover design. We used functional MRI to measure neural responses during these memory encoding sessions, which were separated by a month. Results revealed that corticosteroids' slow effects reduced both prefrontal and hippocampal responses, while no significant rapid actions of corticosteroids were observed. Thereby, this study provides initial evidence for dynamically changing corticosteroid effects on brain regions involved in memory formation in humans.

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Glucocorticoid receptor activation selectively hampers N-methyl-d-aspartate receptor dependent hippocampal synaptic plasticity in vitro

Cited by 76 publications

References 50 publications

Glucocorticoids act on glutamatergic pathways to affect memory processes

Glucocorticoids act on glutamatergic pathways to affect memory processes

Corticosterone time-dependently modulates β-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Dynamically changing effects of corticosteroids on human hippocampal and prefrontal processing

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